PONSZAC 2013 CME

E-BOOK

Editors:

1. Dr. Sameer M Jahagirdar

2. Dr. V R Hemanth Kumar

3. Dr. Debendra Kumar Tripathy

8/23/2013

29TH ANNUAL SOUTH ZONE CONFERENCE &

4TH ANNUAL CONFERENCE, ISA, PUDUCHERRY

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CONTENTS

Author Page

1. Systematic approach to pre-operative assessment and optimization: Dr. Hanumanth Rao

2. Intraoperative Monitoring: What is Necessary, Useful and What is Futile?: Dr. Anita Shenoy

3. Diagnosis and treatment of cardiac complications in the peri-operative setting: Dr. Suresh Nair

4. Pathophysiology of respiratory failure: Dr. Nagmani

Nambiar

5. Techniques for lung separation and conduct of one-lung anaesthesia: Dr. Thomas Koshey

6. Perioperative renal protection: Dr. AL Meenkshee Sundaram

7. Choosing the anaesthetic for ambulatory surgeryGeneral, regional or local anesthesia with sedation?: Dr. U. Murlikrishnan

8. Essentials of neuromonitoring: Dr. Srilata

9. Clinical anatomy for airway managment and vascular access: Dr. Ashok

10. Clinical anatomy for CNB and PNB: Dr. Anuradha

11. Pharmacology of vasoactive drugs: Dr. Venugopal Kulkarni

12. Physiology & pharmacological aspects of neuromuscular block: Dr. M. Kannan

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Systematic approach of pre-operative assessment and

optimization.

Dr M Hanumantha Rao

Senior Professor and Head,

Dept of Anesthesiology and Critical care Medicine

Sri Venkateshwara Instituite of Medical Sciences

Tirupati

The speciality of Anaesthesiology is focused on providing safe and effective anaesthesia during

surgery and other procedures. Because of many advances in anaesthesia technique, anaesthesia

is very safe for the vast majority of patients, including those with heart disease and other serious

medical conditions. In all cases in which a patient will require anaesthesia, the anaesthesiologist

will perform a preoperative evaluation. For very simple, low-risk procedures in completely

healthy young patients, this evaluation may take place immediately prior to your procedure when

you meet your anaesthesiologist on the day of surgery. However, often the surgeon or

anaesthesiologist may want to evaluate you a few days before your surgery. Such evaluations

may take place in a PreAnaesthesia Evaluation clinic. The evaluation occurs during a clinic visit,

it is an opportunity for the anaesthesiologist to learn more about patient general health and how it

may be affected by anaesthesia, and it is also a chance for the patient to ask your

anaesthesiologist questions about the anaesthetic risks and choices.

Definition

Anaesthesia evaluation refers to the series of interviews, physical examinations, and laboratory

tests that are generally used to assess the general fitness of patients scheduled for surgery and to

determine the need for special precautions or additional testing. There is no universally accepted

definition of anaesthesia evaluation as of 2003; however, the Task Force on Preanaesthesia

Evaluation of the American Society of Anaesthesiologists (ASA) has tentatively defined it as

....the process of clinical assessment that precedes the delivery of anaesthesia care for surgery

and for non-surgical procedures. Anaesthesia evaluation is usually discussed in the context of

elective or scheduled surgical procedures rather than emergency surgery.

Anaesthesia evaluation is a relatively recent development in preoperative patient care. Prior to

the 1970s, anaesthesiologists were often given only brief notes or outlines of the patients history

and physical examination written by the operating surgeon or the patients internist. This

approach became increasingly unsatisfactory as the practice of anesthesiology became more

complex. In the last four decades, the introduction of new anesthetics and other medications,

laser-assisted surgical procedures, increasingly sophisticated monitoring equipment, and new

discoveries in molecular biochemistry and genetics have made the anaesthesiologists role more

demanding. During the 1980s and 1990s, some departments of anesthesiology in large urban

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medical centers and major university teaching hospitals began to set up separate clinics for

anaesthesia evaluation in order to improve the assessment of patients before surgery.

Purpose

Anaesthesia evaluation has several different purposes. The information that is obtained during

the evaluation may be used to:

Guide the selection of anesthetics and other medications to be used during surgery.

Plan for the patients postoperative recovery and pain management.

Educate the patient about the operation itself, the possible outcomes, and self-care during

recovery at home.

Determine the need for additional staff during or after surgery.

Minimize confusion caused by rescheduling operations because of last-minute

discoveries about patients health.

Improve patient safety and quality of care by collecting data for later review and analysis.

The ASA has noted that few controlled trials of different approaches to anaesthesia

evaluation have been conducted as of 2003, and that further research is needed.

Description

There are several parts or stages in a typical anaesthesia evaluation. The evaluation itself may be

done in the hospital where the operation is scheduled, or in a separate facility attached to the

hospital. The timing of the evaluation is affected by two major variables: the invasiveness of the

operation to be performed and the patients overall physical condition. An invasive operation or

procedure is one that requires the surgeon to insert a needle, catheter, or instrument into the body

or a part of the body. Surgical procedures are classified as high, medium, or low in invasiveness.

Procedures that involve opening the chest, abdomen, or skull are usually considered highly

invasive. Examples of less invasive procedures would include tooth extraction, most forms of

cosmetic surgery, and operations on the hands and feet.

The patients physical condition is classified according to the ASAs six-point system as follows:

ASA 1. Normal healthy patient.

ASA 2. Patient with mild systemic disease.

ASA 3. Patient with severe systemic disease.

ASA 4. Patient with severe systemic disease that is life-threatening.

ASA 5. Moribund (dying) patient who is not expected to survive without an operation.

ASA 6. Brain-dead patient whose organs are being removed for donation.

As of 2003, the ASA recommends that patients with severe disease be interviewed and have their

physical examination before the day of surgery. Patients in good health or with mild systemic

disease who are scheduled for a highly invasive procedure should also be interviewed and

examined before the day of surgery. Patients in categories P1 and P2 who are scheduled for low-

or medium-invasive procedures may be evaluated on the day of surgery or before it.

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Patient history and records

The first part of an anaesthesia evaluation is the anaesthesiologists review of the patients

medical history and records. This review allows the anaesthesiologist to evaluate the patient for

risk factors that may increase the patients sensitivity to the sedatives or other medications given

before and during the operation; increase the danger of complications related to heart function

and breathing; and increase the difficulty of treating such complications.

These risk factors may include:

Heart or lung disease. These diseases often require the anaesthesiologist to lower the

dosages of sedatives and pain-control medications.

Liver or kidney disease. Disorders of these organs often slow down the rate of medication

clearance from the patients body.

Present prescription medications. These may interact with the sedatives given before the

operation or with the anesthetic agent.

Herbal preparations and other alternative medicines. Some herbal preparations,

particularly those taken for insomnia or anxiety (St. Johns wort, valerian, kava kava)

may intensify the effects of anesthetics. Others, like ginseng or gingko biloba, may affect

blood pressure or blood clotting. It is important for patients to include alternative health

products in the list of medications that they give the doctor.

Allergies, particularly allergies to medications.

Alcohol or substance abuse. Substance use typically affects patients responses to

sedatives and anesthetics in one of two ways. If the patient has developed a tolerance for

alcohol or another drug of abuse, he or she may require an increased dose of sedatives or

pain medications. On the other hand, if the patient has recently consumed a large amount

of alcohol or other mood-altering substance, it may interact with the anesthetic by

intensifying its effects.

Smoking. Smoking increases the risk of coughing, bronchospasm, or other airway

problems during the operation.

Previous adverse reactions to sedatives or anesthetics. A family history of anaesthesia

problems should be included because some adverse reactions are genetically determined.

Age. The elderly and children below the age of puberty do not respond to medications in

the same way as adults, and the anaesthesiologist must often adjust dosages. In addition,

elderly patients often take a number of different prescription medications, each of which

may interact with anesthetics in a different way.

Patient interview

The anaesthesiologist is responsible for interviewing the patient during the anaesthesia

evaluation. The interview serves in part as additional verification of the patients identity; cases

have been reported in which patients have been scheduled for the wrong procedure because of

administrative errors. The anaesthesiologist will check the patients name, date of birth, medical

record number, and type or location of scheduled surgery for any inconsistencies. Although the

anaesthesiologist will ask for some of the same information that is included in the patients

written medical records, he or she may have additional questions. Moreover, it is not unusual for

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patients to recall significant events or details during the interview that were left out of the written

records. The anaesthesiologist will explain what will happen during the operation and give

instructions about fasting, discontinuing medications, and other precautions that the patient

should take before the procedure. The patient will have an opportunity to ask questions about

choice of anesthetic and other concerns during the interview.

Physical examination

The physical examination will focus on three primary areas of concern: the heart and circulatory

system; the respiratory system; and the patients airway. Heart and lung function are evaluated

because surgery under general anaesthesia puts these organ systems under considerable stress.

The usual tests performed to evaluate heart and lung fitness are an electrocardiogram (ECG) and

chest x-ray (CXR). These tests may be omitted if the patient was tested within the previous six

months and the results were normal. If the patient has an ECG and CXR as part of the

anaesthesia evaluation and the findings are abnormal, the doctor may order additional tests of

heart and lung function. These may include stress or exercise tests; echocardiography ;

angiography ; pulmonary function tests (PFTs); and a computed tomography (CT) scan of the

lungs.

Assessment of the airway includes an examination of the patients teeth, nasal passages, mouth,

and throat to check for any signs of disease or structural abnormalities. Certain physical features,

such as an abnormally shaped windpipe, prominent upper incisor teeth, an abnormally small

mouth opening, a short or inflexible neck, a throat infection, large or swollen tonsils, and a

protruding or receding chin can all increase the risk of airway problems during the operation. A

commonly used classification scheme rates patients on a four-point scale, with Class I being the

least likely to have airway problems under anaesthesia and Class IV the most likely.

Laboratory tests

Laboratory tests are categorized as either routine, meaning that they are given to all patients as

part of the anaesthesia evaluation, or indicated, which means that the test is ordered for a specific

reason for a particular patient. Routine preoperative laboratory tests include blood tests and urine

tests. Blood samples are taken for white and red blood cell counts and coagulation studies; tests

of kidney function, most commonly measurements of blood urea nitrogen (BUN) and creatinine;

and measurements of blood glucose and electrolyte levels. Urine samples are taken to evaluate

the patients nutritional status, to test for diabetes or the presence of a urinary tract infection, and

to determine whether the patient is dehydrated. Some hospitals will accept blood and urine tests

performed within six weeks of the operation if the results were within normal ranges. Some

facilities also routinely test urine samples from women of childbearing age for pregnancy.

Indicated laboratory tests include platelet counts, certain blood chemistry measurements, and

measurements of blood hemoglobin levels. These tests are usually performed for patients with

blood or endocrine disorders; persons taking blood-thinning medications; persons who have been

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treated with some types of alternative therapy; and persons who are known to have kidney or

liver disorders.

Consultations

The anaesthesiologist may consult other doctors as part of the anaesthesia evaluation in order to

obtain additional information about the patients condition. Consultations are often necessary if

the patient is very young or very old; is being treated for cancer; or has a rare disease or disorder.

Preparation

Patients can prepare for an anaesthesia evaluation by gathering information beforehand to give

the hospital or clinic staff. This information includes such matters as insurance cards and

documentation; a list of medications presently taken and their dosages; a list of previous

operations or hospitalizations, if any; the names and telephone numbers of other physicians who

have been consulted within the past two years; information about allergies to medications, if any;

the name and telephone number of a designated family member or primary contact; and similar

matters.

Summary and Conclusions.

A preanaesthesia evaluation involves the assessment of information from multiple sources,

including medical records, patient interviews, physical examinations, and findings from

preoperative tests. At a minimum, a directed preanesthetic physical examination should include

an assessment of the airway, lungs, and heart.

***

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Monitoring - what is necessary, useful and futile?

Dr Anitha Shenoy

Professor of Anesthesiology

Kasturba Medical College, Manipal

INTRODUCTION

The way anaesthesia is administered to patients has changed over the years since the time it was first

demonstrated in 1846. The art of anaesthesia has changed to more of science. Similarly, the patients and

public are more aware of anaesthesia. They are more informed, expectations are high and are much more

unforgiving. Errors, especially serious ones will no longer be taken as Gods will. Liabilities are higher

and the need to be alert and appropriate is ever present.

Monitoring of a patient is an integral part of present day anaesthesia. Many of the vital physiological

processes can be measured and monitored. The extent of monitoring depends on the patient, procedure

and facilities available at the hospital. Standards of monitoring have been laid down by various

organisations of every country. They are mostly similar in their essence.

PURPOSE OF MONITORING

Anaesthesia and surgery can alter the patients physiology. The purpose of surgery is to relieve an ailment

and it is reasonable to expect the patient to return to the same condition as before surgery or may be even

better postoperatively. Monitors can be used to measure the baseline status of the patient and then to

follow the trends. Monitors are most often used to monitor physiological functions of the patient. They

may also be used to monitor other equipment.

MONITORING PATIENT: WHAT IS MANDATORY?

The Indian Society of Anaesthesia has also laid down minimum monitoring standards based on the

recommendations of the International Task Force and to suit the Indian conditions. The recommendations

are as follows:

The anaesthesiologist

It is important to note that the most important monitor is the anaesthesiologist. Monitors are only

machines and the data displayed by monitors need to be interpreted appropriately by the

anaesthesiologist. For e.g., the monitor may display presence of ventricular fibrillation but it could be due

to shivering artifacts or some other disturbance, the physician can analyse. Monitors simply cannot

replace a physician.

It is mandatory that every anaesthetic is administered by only a qualified anaesthesiologist. It is required

that the hospital management must make a qualified anaesthesiologist available for every case done under

anaesthesia, be it, general, regional or monitored anaesthesia care. The anaesthesiologist must be present

throughout the procedure and shift the patient to the postoperative care area or intensive care as required.

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If the primary anaesthesiologist cannot be present throughout for any reason, the patient and his condition

may be handed over appropriately to another qualified anaesthesiologist before he leaves.

In addition, since anaesthesia and surgery can be associated with sudden and drastic changes in the

physiology of the patient, and that the anaesthesiologist may need help in dealing with such critical

situations, an additional anaesthesiologist, trained anaesthesia technician, paramedic or a nurse who

knows about these critical conditions and their management must be made available.

Physiological monitors

Although traditionally, anaesthesia was administered and monitored using hand on pulse and clinical

observation of colour and chest movements, it is now mandatory to use some kind of electronic

monitoring for patients. It is mandatory for every patients oxygenation, ventilation and circulation to be

continuously monitored. The following are considered minimum monitoring standards (what is

necessary):

Oxygenation

Monitoring of colour of the skin, surgical field and watching out for cyanosis is not sufficient to detect

hypoxia. Oxygenation of the patient must be continuously monitored using a pulse oximeter, which not

only displays the oxygen saturation and heart rate but must also have a variable pitch and low oxygen

saturation alarm. The use of a pulse plethysmogram is optional.

Ventilation

Ventilation may be monitored using auscultation of breath sounds, observation of chest movements, and

movements of reservoir bag if the patient is breathing spontaneously. It is preferable to use a capnograph

to monitor ventilation but it is not mandatory. Capnographs also help in confirming correct placement of

artificial airways such as laryngeal mask airway and endotracheal tube. Expired volume monitors are

useful. If the patient is being ventilated using a mechanical ventilator, a disconnection alarm to detect

accidental disconnections is necessary.

Circulation

Hand on pulse was mandatory for anaesthesiologists in training 15 20 years ago but this habit is

disappearing fast among the younger generation. While hand on pulse is a good monitor, this alone is

not sufficient or sensitive to detect cardiovascular events. Blood pressure must be measured at least every

five minutes. Heart rate must be displayed continuously and recorded every five minutes. It is mandatory

to use electrocardiogram to monitor for arrhythmia and ischaemia.

Temperature

A method of measuring temperature must be available. Mercury thermometers are limited by their

inability to measure low temperatures, the minimum being 96C. Thermistors are best suited to measure

lower body temperatures.

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MONITORING PATIENT: WHAT IS USEFUL?

Arterial blood gas analysis

A pulse oximeter displays only oxygen saturation of blood and is able to provide early and real time

warning about hypoxia. However, it is not sufficient to monitor oxygenation status when a patient is

breathing high concentrations of oxygen. When the oxygen requirement is high, it may be necessary to

monitor oxygenation status by periodic assessment of partial pressure of oxygen in arterial blood. An

arterial blood gas analysis is also necessary to measure pH and arterial carbon dioxide tension.

Measurement of pH is necessary to evaluate acid-base status.

Invasive arterial pressure

Invasive arterial pressure monitoring is useful and in many situations, considered mandatory when beat to

beat monitoring arterial pressure is required. These may be anaesthesia for special situations such as

cardiovascular and thoracic procedures, procedures associated with major haemodynamic changes or fluid

shifts and in patients with major cardiovascular co-morbidities. It is also necessary when potent

cardiovascular drugs such as inotropes, vasopressors or vasodilators are required.

Central venous pressure

Monitoring of central venous pressure is useful for anaesthesia for special situations such as

cardiovascular and thoracic procedures, procedures associated with major haemodynamic changes or fluid

shifts and in patients with major cardiovascular co-morbidities. In addition, they may be used when

peripheral intravenous access is not available, long term antibiotic use or chemotherapy is expected or the

patient is in need of potent vasoactive drug infusion.

Pulmonary artery pressure

Pulmonary artery (PA) catheter insertion and interpretation of data is useful mostly in cardiac surgery.

Even in cardiac surgery, it is often limited to patients with left ventricular dysfunction, especially if

transoesophageal echocardiography is available. PA catheters capable of measuring pulmonary capillary

wedge pressure and pulmonary arterial pressure only are available. Addition of a thermistor at its tip gives

it the capability of measuring cardiac output by thermodilution method.

Cardiac output

Measurement of cardiac output, either continuous or intermittent using a pulmonary artery catheter is

limited to cardiac surgery. However, with the advent of less invasive cardiac output monitors such as

Flotrac or oesophageal Doppler, measurement of cardiac output for guiding fluid responsiveness in

increasingly used for surgeries associated with major fluid shifts. Their usefulness in influencing outcome

is yet to be proven.

Anaesthetic gas analysers

The concentration of anaesthetic gases in the inspired and expired gases can be measured and displayed

continuously. Although there are several methods of measurement, infrared analysers are most useful.

The gases from breathing system are continuously aspirated by a side stream method and analysed inside

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the monitor. The monitor contains algorithms to display minimum alveolar concentration of anaesthetic.

This is very useful in titrating anaesthetics, especially when low fresh gas flows are used. This may be a

very useful tool to avoid awareness under anaesthesia. A record of these values may also be useful in the

event of lawsuits against anaesthetist.

Depth of anaesthesia monitors

Gauging the depth of anaesthesia has largely remained an art. Great reliance has been placed on clinical

parameters such as heart rate, blood pressure, sweating and tearing indicative of sympathetic response to

detect awareness, particularly if the patient is paralysed. Movement of the patient is useful in

spontaneously breathing patients. Anaesthetic gas analyser is useful in measuring concentration of

anaesthetic delivered to the patient. More objective monitoring of depth of anaesthesia based on

electroencephalogram can be done using BIS index monitor or entropy. These monitors actually measure

the effect of anaesthetics on the brain rather than merely display anaesthetic concentrations. Thus they are

more likely to be useful as indicators of depth of anaesthesia. These monitors display numbers 0 100,

where in 40 60 is considered adequate anaesthesia, < 40 is deep anaesthesia and > 60 is light

anaesthesia. These monitors can be influenced by other factors such as hypothermia and are not entirely

accurate. Their role in influencing outcome is also not proven.

Transoesophageal echocardiography

Transoesophageal echocardiography is most useful in cardiac surgery for early detection of left

ventricular dysfunction, assessment of adequacy of valve repairs, evaluation of ventricular filling,

effusions and tamponade etc. Visual and real time assessment of the ventricular and valvular function is

much more informative than indirect measurements such as chamber pressures. This information may be

more useful to the surgeon for decision making. However, the equipment is very expensive and special

training is required to obtain the correct images and interpret them limiting their routine use.

Mixed venous oxygen saturation

Continuous or intermittent monitoring of mixed venous oxygen saturation (if pulmonary artery catheter is

in-situ) or central venous oxygen saturation (obtained through a special central venous catheter) is useful

to titrate therapy in patients in septic shock. This is part of the surviving sepsis guidelines.

To understand the usefulness of central venous oxygen saturation, reference may be made to Ficks

equation. Ficks equation states that the cardiac output is equal to the total oxygen consumption divided

by arteriovenous oxygen content difference. It may be written as follows:

CO = VO2 / C (a v) O2, where CO represents cardiac output, VO2 = oxygen consumption,

C(a v)O2 = Arteriovenous oxygen content difference.

SvO2 can be used to derive cardiac output when oxygen consumption is normal and constant. It

can be used to monitor oxygen extraction ratio which is the ratio of oxygen consumption and

delivered oxygen. The normal oxygen extraction ratio is 20 - 25%. The critical oxygen extraction

ratio is 70% in normal individuals, below which anaerobic metabolism will occur. This

corresponds to a venous oxygen saturation of 30% (SvO2 = 1 ER). One cannot survive for

more than a few minutes to an hour with venous oxygen saturation less than this value.

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In critically ill patients, this critical oxygen extraction ratio may fall to 50%, corresponding to

SvO2 < 50%. Thus, SvO2 may be interpreted as follows:

> 70% - Normal

< 40 - 50% = Low, correct immediately

< 30% - Death imminent

50 70% - Interpret after correlation with clinical picture

When low venous oxygen saturation is seen, the cardiac output, haemoglobin or arterial oxygen

saturation have to reviewed and optimized. Attempts may be made to reduce oxygen demand or

consumption by sedating or paralysing the patient.

Measurement of venous oxygen saturation can be used to guide therapy in the perioperative

period. Reduced oxygen saturation may be due to reduced oxygen delivery due to factors such as

alveolar hypoxia, anaemia, hypovolaemia or heart failure. It may also be due to increased oxygen

consumption due to factors such as pain, agitation, pyrexia, shivering or respiratory failure. Any

intervention used to improve venous oxygen saturation requires clear understanding of the

pathophysiology of such a change in that patient. Judicious use of venous oxygen measurements

can be made to improve perioperative management and outcome.

Mixed venous oxygen saturation gives a better idea about global oxygen consumption but

requires insertion of pulmonary artery catheter. ScvO2 generally overestimates SvO2 by 3 8%,

since the blood from coronary sinus as well as inferior vena cava may not have mixed with the

superior vena caval blood sample. However, if the tip of the central venous catheter is in the

right atrium, ScvO2 overestimates SvO2 by only 1% and is an excellent surrogate of SvO2.

Whether SvO2 needs to be measured continuously or intermittently depends on clinical picture of

the patient. If the patient is very unstable and is in septic shock, it may be more useful to have

continuous measurement of SvO2 (ScvO2) whereas when the patient is more stable, intermittent

measurement may suffice.

Defibrillator

A defibrillator must be available at every hospital and is considered essential resuscitation

equipment.

MONITORING EQUIPMENT

Oesophageal stethoscope

This is a long tube similar to a nasogastric tube but with a noninflatable balloon at the tip. It is inserted

blindly into the oesophagus either through the mouth or nose in an anaesthetised patient. The proximal

end of the tube has a stethoscope which can be used to listen to both heart and breath sounds. It is very

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useful when there is no access to the chest during surgery for auscultation, especially where power

outages are common and no other monitoring is possible.

Precordial stethoscope

This is an ordinary stethoscope fitted with along tubing. This is commonly used in infants and children

but can be useful in adults also. The diaphragm is taped on to the precordium so that the heart and breath

sounds can be auscultated simultaneously. It is very useful when there is less access to the chest during

surgery for auscultation, especially where power outages are common and no other monitoring is

possible.

Oxygen analysers

The Indian society of anaesthetists recommends that anaesthesia machines should have hypoxic guard

where in delivery of not less than 25% oxygen at all times can be ensured. If anaesthesia machines

without hypoxic guard are being used, an oxygen analyser must be used to guard against delivery of

hypoxic mixture to patients.

Airway pressure monitors

Airway pressure monitors must be used mandatorily to detect ventilator disconnection when mechanical

ventilators are used to ventilate patients under anaesthesia. A continuous display of the peak and mean

airway pressure is very useful in assessing the compliance and resistance of the respiratory system. Any

change in the airway pressure due to surgery or comorbid disease can be detected early and treated

appropriately. The effectiveness of the treatment can also be monitored.

Tidal volume monitors

Monitoring the tidal volume along with airway pressure provides more useful information about the

condition of the respiratory system. When mechanical ventilators capable of providing pressure controlled

ventilation are used, changes in delivered tidal volume due to changes in airway resistance and

compliance must be monitored. Any change in the airway pressure due to surgery or comorbid disease

may be detected early and treated appropriately. The effectiveness of the treatment can also be monitored.

MONITORING: WHAT IS FUTILE?

A monitor should not be used only because it is available and it is possible to use it. Every monitor can be

useful provided it is used correctly. Any monitoring is futile if there is no indication to use it, the user is

not familiar with its use or wrong values are followed. If risk-benefit analysis is done for every monitor

used on a patient, no monitoring is futile. Furthermore, it can be stated that all monitoring can turn to be

futile if the most important monitor, the anaesthesiologist is not present, present but not vigilant or

present, vigilant but does not know how to react to a given critical situation. A monitor cannot simply

replace a physician.

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SUMMARY

Every anaesthetic begins with monitoring and ends with monitoring, the intent being to keep the patient

safe through the stress of surgery and anaesthesia. It helps to detect and treat appropriately any altered

physiology due to disease and surgery. The anaesthesiologist is the most important monitor and eternal

vigilance describes what he/she does during most of the anaesthetic. While some monitoring is

mandatory, it can and should be escalated to be appropriate and proportionate to the condition of the

patient.

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Perioperative cardiac complications: myocardial ischemia

recognition and management.

Dr. Suresh Nair

Professor

Amrita Institute of Medical Sciences

Cochin, Kerala

Perioperative myocardial infarction (PMI) is one of the most important causes for short and long term

morbidity and mortality associated with non cardiac surgery. Prevention of a PMI is therefore of great

importance in improving the overall outcome after non cardiac surgery. In the last few years, extensive

research has been conducted into the causes of PMI. Yet, the exact causes of PMI remain an area of

debate and controversy. In addition, identifying PMI is difficult as the classical changes associated with

myocardial infarction (MI) in the non surgical settings are often missing. This article deals with the

probable causes of PMI, the diagnostic criteria and the preventive and treatment measures.

Perioperative myocardial infarction.

PMI often has peculiarities:

1. PMI peaks in the immediate postoperative period and is often associated with MI and cardiac

complication. The majority of the MI presents during the first 4 days after surgery and 90% by

day 7 after surgery (2). Intraoperative plaque rupture is less common and infrequently associated

with PMI. This puts to rest the earlier argument that the type of anesthesia (general or regional

anesthesia), if properly delivered, is not a risk factor for high risk cardiac patients undergoing

non-cardiac surgery.

2. PMI is almost exclusively associated with ST depression type myocardial ischemia. ST elevation

type MI which is almost exclusively seen in the non-surgical setting is uncommon in the

perioperative period.

3. PMI is often silent and often a NQMI is seen rather than a QMI.

4. The majority of the PMIs occur within the first 48 hours after surgery

5. Mortality after PMI is < 10-15%, similar to the mortality after non-surgical NQMI. This is in

contrast to earlier concerns that PMI is associated with very high mortality.

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The above statements gives rise to the following questions concerning PMI: Is the pathophysiology of

PMI different from that of the non-surgical MI? Does the understanding of the pathophysiology affect the

ability to prevent, diagnose or treat MI?

Pathogenesis of MI in non surgical settings.

One of the central concepts in the pathogenesis of MI is the distinction between stable and unstable

plaques. Studies have shown that a rapidly growing atheromatous plague consists of a large inner core

composed of substantial thrombogenic lipids and macrophages and covered by a thin fibrous plague. The

thin fibrous plague shows signs of inflammation, degradation and repair of its matrix. A stable plague on

the other hand is made of a thin fibrous core and covered by a thick fibrous matrix. In the unstable plague,

the inflammatory process that leads to erosion of the fibrous matrix exceeds the reparative process, it

becomes unstable and susceptible to fissuring and rupture of the fibrous cap.

Cycles of fissuring and disruption of the fibrous cap, leading to mild degrees of thrombosis, platelet

aggregation, myocyte migration and healing of the fibrous matrix are believed to be part of the growing

atheromatous plague. By this process, an atheromatous plaque may grow to critical or even complete

closure of major coronary arteries without causing MI as the process is often accompanied by

simultaneous growth of collateral coronary circulation. Rupture of the unstable plague with large lipid

core may also occur exposing the thrombogenic material to the circulation. Rupture of atheromatous

plagues may occur secondary to shear forces acting on it from within the lumen or inflammatory and

degradation process within the plague itself. Once an atheromatous plaque with large thrombogenic core

ruptures, the interaction between the thrombogenic material and blood components may result in

thrombus generation and complete occlusion of the vessel.

The differences in the clinical picture of the various acute coronary syndromes (ACS) can be explained on

the basis of the degree and duration of plague rupture, thrombus deposition and coronary occlusion.

Minor repeated plague rupture accompanied by relatively short term or partial coronary occlusion by

thrombosis or vasoconstriction causes unstable angina pectoris (1). More severe plague rupture with

prolonged but reversible coronary occlusion in patients with good coronary collateral circulation causes

non Q wave myocardial infarction (NQMI). In patients with severe and prolonged coronary occlusion in

major territory with poor coronary collateral circulation lead to Q wave myocardial infarction (QMI).

The sudden and rather non random causes of rupture of plague and MI are probably related to:

1. Plague disruption triggered by surges in sympathetic activity and associated with increase in heart

rate (HR), blood pressure, contractility and coronary blood flow

16 | P a g e

2. Coronary thrombosis on previously ruptured or complicated plagues caused by fluctuations in

systemic thrombotic activity because of platelet hyperaggregability, hypercoagulability and

impaired fibrinolysis.

3. Vasoconstriction either locally around an unstable coronary plague or generalized secondary to

sympathetic stimulation

Mechanism of perioperative MI.

Two distinct mechanisms can lead to PMI: acute coronary syndrome (Type 1) and prolonged oxygen

demand supply imbalance (type 2) in the presence of stable coronary artery disease (3).

Type 1 : Acute coronary syndrome.

ACS occurs when an unstable or vulnerable plaque undergoes fissuring, rupture leading to acute

thrombosis, ischemia and infarction. The following conditions are known to influence the onset of plaque

rupture during the perioperative period

1. Physiological and emotional stress is thought to promote sympathetic discharge, coronary

vasoconstriction and prothrombotic states in the immediate postoperative period.

2. Tachycardia and hypertension common in the immediate postoperative period may exert shear

stress, leading to rupture of the plaque.

3. Increased postoperative pro-coagulants (fibrinogen, factor VIII coagulant, von Williebrand factor

and 1-trypsin) increased platelet activity, decreased endogenous anticoagulants (protein C,

antithrombin 111, 2 macroglobulin) have been reported. Postoperative hypercoagulability is

notorious for venous complications precipitated by stasis and immobilization.

It is generally believed that the risk of MI posed to the patients with a given coronary artery disease is

directly related to the severity of the coronary stenosis. However, studies that looked at the degree of

coronary stenosis before and after an AMI, showed the majority of the culprit coronaries had a lesion of <

70% (4). This discrepancy between angiographic evidence of coronary severity and likelihood of MI is

explained by the inability of the angiogram to identify unstable plaques that are at high risk of rupture and

distinguish them from significant but stable coronary plaques. These findings also substantiate the fact

that younger and less mature plaques are the ones most likely to rupture and cause acute MI.

Type 11: Oxygen supply-demand imbalance.

Postmortem studies in patients who developed PMI showed that the perioperative events that lead to PMI

was evenly distributed between plaque rupture and oxygen demand-supply imbalance. It is possible that

17 | P a g e

in the perioperative settings, the later may have a greater role in the cause of PMI. This statement is

further substantiated by the finding that there was no evidence of plaque rupture in 83% of patients who

developed PMI within the first 3 days and 77% of patients in the first 4 days. This could mean that

oxygen demand-supply imbalance is the predominant cause of PMI in the first few days after surgery (5).

Plaque rupture as a cause of PMI was evenly distributed over the entire postoperative period. Although

PMI occurred in the background of significant coronary artery disease, total coronary occlusion with

thrombus occurs in only 50% of the patient. This suggests that low flow states secondary to significant

coronary stenosis is an important contributor to the cause of PMI.

Perioperative hyopertension is uncommonly associated with perioperative MI while perioperative

hypotension is associated with an increased incidence of MI, cardiac arrests and cardiac deaths. The

duration of hypotension may be a significant factor in the incidence of perioperative MI.

Studies in patients with significant CAD undergoing surgery has shown that silent, heart rate related ST

segment depression is common postoperatively and is associated with in-hospital and long term mortality

and morbidity (6, 7). Postoperative cardiac complications including sudden death occurred after

prolonged, silent ST-segment depression. These changes were reflected in cardiac troponin levels.

Cardiac troponin levels are elevated after prolonged or transient ST depression in the postoperative

period. The severity in elevation of the cardiac troponin levels correlated with the duration of ST segment

elevation. ST segment elevation was very uncommon. Hence, prolonged ST segment depression type

myocardial ischemia is the most common cause of PMI.

It has also been shown that low level but prognostically significant elevations in troponin levels occur in

high risk cardiac patients without any significant ECG signs of ischemia. Troponin levels above the cut

off value (>0.03 ng/ml) occurred in 24% of patients early after vascular surgery, only 32% of whom had

ECG evidence of ischemia whereas among 8.7% patients with PMI (troponin >0.1 ng.ml) 88% had

ischemia on continuous ECG monitoring (8). Higher troponin levels correlated with longer duration of

ischemia. Thus, type 11 PMI spans a spectrum ranging from silent, minor cardiac injury with low level

elevation in cardiac troponin and low incidence of ST changes to prolonged overt changes in multiple

ECG leads, marked elevations in cardiac troponin and PMI.

Tachycardia is the most common cause for postoperative myocardial oxygen demand-supply imbalance

mediated ischemia (3). Increase in HR in patients with significant coronary artery disease can lead to

subendocardial ischemia through the imbalance created by the increase in oxygen demand while reducing

the oxygen supply through shortening of the diastolic interval. HR of 80-90 is poorly tolerated by high

risk cardiac patients having resting HRs of 50-60, leading to prolonged ischemia. Hypotension,

18 | P a g e

hypertension, anemia, hypoxemia, hypercarbia aggravate coronary ischemia. Hypotension more

commonly leads to ischemic changes than hypertension. Prolonged intraoperative hypotension (> 20

mmHg reduction in mean arterial pressure for > 60 min) results in significant increases in myocardial

infarctions, deaths and cardiac arrests. Stress induced and ischemia induced coronary vasoconstriction

further impairs cardiac perfusion.

QMI versus NQMI.

Differentiation between NQMI and QMI is important to understand the pathophysiology of PMI. The

preponderance of NQMI in the postoperative settings suggests the role of prolonged ischemia rather than

thrombotic occlusion as cause of PMI. Some of the well known concepts of NQMI include:

1. NQMI involves a smaller volume of myocardial tissue than QMI

2. Short term (in-hospital) mortality of NQMI is less than that of QMI.

3. NQMI has a greater incidence of recurrent angina than QMI and this reflects the larger volume of

jeopardized myocardium involved with NQMI.

4. The long term mortality and morbidity of NQMI is at least equal if not higher than QMI.

Since it is not possible to distinguish whether a patient will develop a QMI on arrival in the emergency

room, the concept of NQMI versus QMI is being regarded as meaningless by many cardiologists. The

concept of ST elevation versus ST segment depression MI is more important as the management criteria

at the moment are entirely different.

Diagnosis of PMI.

Diagnosis of PMI in the operating room or in the immediate postoperative period is difficult and often

missed. As per the World Health Organization, at least 2 of the 3 criteria mentioned must be fulfilled

before a diagnosis of MI can be made. These include i) typical ischemic chest pain ii) increased serum

creatine kinase (CK- MB isoenzyme, and iii) typical ECG changes.

The standard ECG used in the OR or in the ICU often uses a high degree of filter to prevent wandering of

the signals up and down the screen. Unfortunately, low frequency filtering may distort the ST segment

and render it unusable for ST segment analysis for ischemia. Secondly, standard calibration of the ECG

signal is 1 cm/mV. At this calibration 1 mm of ST segment depression equals 0.1 mV. However, a 1 mm

change in ST segment is very difficult to see on the monitor. Thirdly, the standard leads that are

monitored in high risk cardiac patients are often the Lead 11 and V5. Although the combination is good,

many of the changes that occur in the perioperative period is often seen in V2-V4 that may be missed.

Finally, anaesthesiologists being fully occupied within the operating room may miss the changes

19 | P a g e

appearing on the monitor. Fortunately automated ECG segment analysis has overcome many of these

limitations.

The development of assays for cardiac troponin T (cTnalT) and I (cTnI) that are highly specific and

sensitive for myocardial injury formed the basis of the revised definition of MI by Universal Definition of

Myocardial Infarction (9). According to this criteria the definition of MI may be entertained when i)

definition of a rise and or fall of cardiac biomarkers (preferably troponin) with at least one value above

the 99th percentile of the upper reference limit together with evidence of myocardial ischemia with at least

one of the following a) symptoms of ischemia b) ECG changes indicative of new ischemia (new ST

changes or LBBB) c) development of pathological Q waves on ECG d) imaging evidence of new loss of

viable myocardium or new regional wall motion abnormality.

Debate continues at arriving at an appropriate cut off value for cardiac troponin which can lead to a

clinically relevant diagnosis of MI. The question also arises that when a diagnosis is made based on

biomarkers alone whether it would lead to an overestimation of the incidence of PMI or when traditional

definitions are used for diagnosis of PMI it would lead to an underestimation of the incidence of PMI.

Initial cut off values (cTnT > 1ng/ml and cTnI >0.1 ng/ml) were based on patient population which had

clinically relevant MI. However, subsequent studies have shown that even minimal increases in cardiac

troponin levels without any ST changes are associated with adverse cardiac outcomes. It has been

suggested that due to the specificity of cardiac troponin, in the presence of documented myocardial

ischemia, even minor increases in cardiac troponin above the 99th percentile normal should be considered

as MI. Postoperative increases in cardiac troponin (cTnT) correlated with cardiac morbidity after vascular

surgery. In 229 patients, an increase in postoperative cTnI above 0.15 ng/ml within the first 3 days was

associated with a 6-fold increase in mortality and a 27-fold increase in risk for MI (10). A dose response

relationship was observed between the elevation of cTnI and mortality. Patients with postoperative cTnI

levels above 0.30 ng/ml had significantly higher mortality than patients with cTnI levels < 0.35 ng/ml.

A minor increase in cardiac troponin levels (cTnI > 0.6 and or cTnT > 0.03 ng/ml) or an increase in CK-

MB (CK >170 IU or CK-MB/CK >5%) in the first 3 days after surgery should be considered as

significant and is indicative of long term mortality.

Transesophageal echocardiography is a very sensitive to identify RWMA. When new RWMA persists

through the end of surgery, they should be assumed to predict postoperative cardiac complications. The

major disadvantage with TEE is that it cannot be used in the awake patient in the ICU where transthoracic

echocardiography will have to be used.

20 | P a g e

Clinical signs and symptoms suggestive of PMI.

Other clinical signs of PMI which manifest usually late after a PMI includes fluctuations in blood

pressure, tachycardia or heart blocks. An emergency 12-lead ECG may be diagnostic. The

anesthesiologist should in the meantime rule out any anesthetic or pain related causes of hypertension or

hypotension, tachycardia. In patients with cardiac risk undergoing high risk procedures it is recommended

that an ECG should be obtained at baseline, immediately after surgery and the first two postoperative

days.

Prevention of PMI.

Beta blockers (BBs) are considered as top priority cardio-protective agents in high risk cardiac patients.

Many beneficial effects, including anti-arrhythmic, anti-inflammatory, altered gene expression and

receptor activity and protection against apoptosis have been attributed to the beneficial effects of BBs.

One major cardio-protective mechanism attributed to BBs include their ability to prevent plaque rupture

by reducing mechanical and hemodynamic stress on vulnerable plaques (1). In addition, BBs prevent MI

by preventing prolonged, stress induced (or tachycardia induced) ST depression type myocardial ischemia

even in the presence of stable yet severe non-vulnerable plaques. All BBs except those with intrinsic

sympathomimetics activity reduce mortality in heart failure and MI probably by reducing the infarct size

and reduction of ventricular arrhythmias.

Catecholamines increase each of the four components of cardiac activity (HR, contractility, preload and

afterload). BBs have the potential to reduce myocardial oxygen consumption by decreasing sympathetic

tone and myocardial contractility, in turn reducing HR and arterial pressure. Furthermore, by reducing

beta receptor mediated release of intra-cardiac norepinephrine during ischemia, they attenuate exercise

induced coronary vasoconstriction.

Effect on perioperative cardiac mortality.

There are two studies that have set the ignited the perioperative protective effects of BBs (11, 12). In the

first study 200 patients at risk of cardiac events were given intravenous atenolol just before major surgery

and continued till discharge or 7 days postoperatively (11). The primary end points of study were cardiac

events and cardiac deaths during a two year study period. The BB group showed a 55% relative risk

reduction (10% Vs 21%) during this period which was primarily related to reduction in cardiac deaths

during the first 6 months after surgery. The study was criticized for many reasons (13). The study took

into account adverse events only after discharge from the hospital although 6 patients died in the hospital.

If these patients were taken into account then the beneficial effect on BBs would have lost statistical

21 | P a g e

significance. Female gender was under-represented in the study. The potential for acute BB withdrawal

was not accounted as eight patients in the control group were deprived of their BBs due to

randomization, There was a trend towards more effective cardiac therapy in the atenolol group whereas

there was a tendency for more sick cardiac patients in the control group.

A subsequent study looked at 1352 patients for cardiac risk factors undergoing major vascular surgery

(12). 846 patients were identified with at least one cardiac risk factor of which 173 patients had a positive

Dobutamine Stress Echocardiography (DSE). 61 of these patients were excluded as they had severe

coronary artery disease or because they were already taking BBs. The remaining 112 patients were

randomized to either a group receiving bisoprolol started at least 37 days before surgery or placebo group.

The study showed a surprising 10-fold decrease in the perioperative cardiac events in the bisoprolol

protected group compared with the standard group. The study was criticized for its small sample size,

early termination of study as the interim analysis showed a large treatment effect and because the study

was not blinded (13). A large complication rate in the standard group was also questionable.

The Polderman study has subsequently undergone a number of re-analysis. Taking all these reviews into

consideration, it can be suggested that BBs would be helpful in the vast majority of patients with at least

one cardiac risk factor undergoing major surgery. Perioperative BBs would not be of benefit in patients

without any cardiac risk factors undergoing major surgery. BBs would reduce the incidents of cardiac

events in patients with three or more clinical risk factors (defined as age > 70 years, current angina, prior

MI, congestive heart failure, diabetes mellitus, renal failure or past cerebrovascular event). Within this

subset of patients with three or more cardiac risk factors, patients who had less than four new regional

wall motion abnormalities on DBE were again protected by the use of BBs. In a small subset of patients

with more than three cardiac risk factors and more than 5 new RWMA on DSE is unlikely to be protected

by BBs alone and may require additional coronary angiography and coronary intervention (13).

The POISE study in 2009 with > 8000 patients showed that although the acute use of BBs was

associated with reduced cardiac events (PMI by 26%), the mortality was higher (by 31%) and incidence

of stroke was higher (by 100%) in patients receiving extended release BBs in the perioperative period

(14). The increased mortality and morbidity was associated with increased incidence of hypotension and

bleeding. BBs aggravate hypotension during surgery and interfere with the ability to maintain adequate

cardiac output during active bleeding, anemia or infection. Consequently there is a strong debate

regarding the use of BBs during the perioperative period.

Following the POISE study publication, the ACC / AHA came up with a focused update on perioperative

BB therapy (15). They have mentioned that BB therapy titrated to HR and blood pressure may be useful

22 | P a g e

in patients undergoing vascular surgery in whom preoperative assessment identifies high cardiac risk as

defined by the presence of one or more clinical risk factor (Class 11A). They also mention that routine

administration of BB in the absence of dose titration is not useful and may be harmful in patients who are

not taking BBs currently (Class 111)

Should BBs be used along with other sympatholytic therapies?

The safety of administering BBs along with thoracic epidural or 2 agonists has not been established. It

is conceivable that the synergistic effect between the two classes of drugs can cause unacceptable

hypotension or bradycardia counteracting any potential benefit of BBs alone. If the combination is used

it should be with extreme caution.

Is there a BB of choice for the perioperative period?

The beneficial effect on BBs is related to its ability to block or suppress the adrenergic response during

surgery and in the postoperative period. In this respect, the type of BB with respect to their receptor

affinity, lipophilicity etc should not be an issue. In clinical practice, one would prefer to use a BB which

has been used in actual trial. The most common of these are the cardio selective BBs like metoprolol,

bisoprolol or atenolol.

When should perioperative BB be started?

Based on the outcome of POISE study and the studies discussed earlier, BBs should be started well in

advance of any planned surgery. This may be as early as one month before surgery or as short as 7-10

days before surgery.

What should be the therapeutic goal?

The primary aim of perioperative BB therapy should be to titrate the HR. Perioperative BB therapy

should be aimed at achieving a target HR of 50-60 (resting). Postoperative HR should be maintained <

80/minute or 20% less than the preoperative ischemic threshold.

For how long should BB therapy be continued?

For patients who have been placed on BB therapy with clear indications, it is preferable to continue with

BB therapy indefinitely. In patients who have been placed on BB with less clear indications, therapy

should be continued for at least the time of hospitalization and preferably up to a month after surgery. In

patients who are to be withdrawn from BBs, the dose should be gradually reduced to avoid any

withdrawal syndromes.

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Is routine BB therapy continued preoperatively as effective as acutely initiated closely monitored HR

targeted perioperative BB therapy?

There is no definite data to substantiate this point. However, based on analysis of Polderman study, there

is suggestive evidence that chronic BB therapy is as effective as acutely initiated, closely monitored, HR

targeted therapy initiated before surgery. Ultimately, the protective effect of BB therapy is related to the

target HR achieved.

Who should receive perioperative BB therapy?

In high risk patients with more than 3 clinical risk factors and positive non-invasive cardiac stress test

(DSE), BBs alone is unlikely to be protective and further coronary intervention is required. In high risk

patients with negative stress testing or in patients with intermediate risk factors, with good functional

capacity and no evidence of angina or peripheral vascular disease, BBs would be helpful in reducing

perioperative morbidity and mortality. In patients with intermediate risk factors but poor functional

capacity or evidence of angina or PVD, additional coronary intervention may be required. BBs are

unlikely to give any additional benefit in patients with no cardiac risk factors.

lpha-2 agonists.

Alpha 2 agonists may be useful as they attenuate perioperative hemodynamic instability, inhibit central

sympathetic discharge, reduce peripheral NE release and dilate post stenotic coronary vessels. However,

the beneficial effects of these group of drugs are seen only with drugs having rate limiting effects.

Antiplatelet therapy.

Aspirin which blocks the thromboxane pathway is a weak but useful antiplatelet agent. The continued use

of aspirin alone is not associated with significant perioperative bleeding while the beneficial effects of the

drug are substantial. Clopidogrel, the thienopyridine has more severe bleeding issues if continued into the

perioperative period. As per the present guidelines, dual antiplatelet therapy (clopidogrel with aspirin)

should be continued for at least 4 weeks after bare metal stent implantation and at least for one year after

drug eluting stent placement. Elective surgery during this period is discouraged. If discontinuing

antiplatelet therapy is mandatory, aspirin should be continued and bridging therapy should be

considered during the interim period. Glycoprotein 11b/111a inhibitors (abxicimab, tirofibran or

eptifibatide) may be considered in this situation.

24 | P a g e

Statins.

Pleiotropic effects of statins independent of their lipid lowering effects have been found to be useful in

preventing myocardial ischemia. These effects include reversal of endothelial dysfunction, modulation of

macrophage activation, immunological effects and anti-inflammatory, anti-thrombotic and anti-

proliferative actions. Aggressive statin therapy in patients who suffer myocardial ischemia is associated

with significant reduction in the composite end point of death, non fatal myocardial infarction, cardiac

arrest with resuscitation and recurrent symptomatic myocardial ischemia. If statins are withdrawn after an

acute coronary syndrome, mortality rates and non fatal infarction rates are increased compared to patients

who continue receiving them.

Perioperative management.

The importance of preventing tachycardia in the perioperative and postoperative period cannot be over

emphasized. All causes of tachycardia, hypotension, hypertension, anemia and pain should be effectively

treated. Treatment of tachycardia with hypotension is particularly challenging and needs a complete

understanding of the patients baseline and periperative myocardial, vascular and coronary physiology.

Vasopressors to maintain blood pressure with BBs to reduce HR along with volume replacement, along

with attention to pain and respiratory care can resolve many of the situations. In our own unit we use

intravenous nitroglycerine as an infusion in all patients with known coronary artery disease during the

perioperative period. Emergency coronary intervention, use of glycoprotein 11b/111a receptor inhibitors

or anticoagulants are rarely required in the postoperative period and may be dangerous because of the risk

of bleeding unless ST segment elevation or intractable cardiogenic shock sets in.

Anemia independently predicts mortality within 30 days in coronary patients. There is considerable

controversy regarding transfusion requirements in high risk cardiac patients especially when the

hematocrit is between 25%-33%. Hemodynamically unstable postoperative patients with ischemia may

benefit from transfusions. Pain if present should be treated with narcotics preferably fentanyl or

morphine. Adequate pain relief will suppress the adrenergic surge seen with intense pain and which is

also characteristic of early stages of PMI and thereby reduce myocardial oxygen consumption.

Treatment of established myocardial ischemia.

Myocardial ischemia should be viewed with the same degree of urgency as hypoxemia and hypotension

as there is imminent risk of death. There is no established management protocol for the management of

intraoperative or immediate postoperative onset of myocardial ischemia. In general, the principals would

include i) evaluation and correction of anaesthetic depth, and adequacy of pain management and

25 | P a g e

ventilation (if patient is in OR) ii) correction of hemodynamic instability iii) anti-angina therapy and iv)

institution of invasive maneuvers like intra-aortic balloon pump or coronary angioplasty.

The adequacy of anesthetic depth should be evaluated if the ischemia onset in within the OR. The depth

of anesthesia, adequacy of pain relief and ventilation status should be assessed. In adequate alveolar

ventilation can result in hypercarbia and sympathetic stimulation which can result in increased HR and

blood pressure both of which can precipitate myocardial ischemia.

Management of HR takes priority as an increase in HR is associated with increased myocardial oxygen

demand while the coronary supply becomes inadequate due to shortening of the diastolic interval.HR may

be controlled by administration of fentanyl or titrated doses of BBs. Use of BBs in this situation should

be with caution as inadvertent high dose may result in bradycardia and hypotension which may be

detrimental in the final outcome. Esmolol with its short duration of action is a favored drug although most

centers now use intravenous metoprolol quite effectively.

The etiology of hypotension is the key to determining the management strategy. Hypovolemia should be

managed by volume therapy. Even in cases where a central venous pressure is not available for

assessment and there is no obvious blood loss a fluid challenge would not be a wasted effort. Undue

vasodilatation causing hypotension may be managed by additional vasopressor administration

(phenylephrine). While adequate filling is a prerequisite, the negative impact of overfilling should also be

understood. The coronary perfusion pressure is the difference between the aortic diastolic pressure (ADP)

and the left ventricular end diastolic pressure (LVEDP). In many coronaries with significant obstruction

the upper pressure may be much less than the actual ADP and if the LVEDP is high because of over

filling, there may be practically no coronary perfusion.

Reduction in myocardial oxygen consumption is also a target. This may be reduced by reduction of

contractility as well as reduction in ventricular wall tension. Myocardial contractility can be reduced with

drugs like BBs or reduction in afterload (inhalation anesthetics, afterload reducing agents like milrinone)

although this may be detrimental when the ADP becomes too low. Wall tension can be reduced by

controlled volume therapy or use of intravenous nitroglycerine.

Role of intravenous nitroglycerine.

Intravenous nitroglycerine has a rapid onset and short duration of action. It reduces preload to the heart,

reduces LVEDV and ventricular wall tension. Reduction in LVEDV should reduce the left ventricular end

diastolic pressure and myocardial wall tension. Nitroglycerine also dilates the large epicardial coronary

arteries even when significant stenosis is present. These beneficial effects should enhance the coronary

26 | P a g e

perfusion. If nitroglycerine fails to improve the ischemic changes and tachycardia is persisting, then

titrated doses of BBs may be used.

Intra-aortic balloon pump.

Even in the non cardiac setting an IABP may be useful. It augments the diastolic blood pressure and

thereby increases the coronary perfusion. The sudden deflation of the balloon during the onset of

ventricular systole results in significant reduction in LV afterload and reduces the myocardial oxygen

consumption. The only situation where IABP may not be useful is when there is undue drop in systemic

resistance when the augmentation may not adequately improve coronary flow.

Role of coronary intervention.

In the perioperative setting a conservative approach is recommended. In case of STEMI, although

fibrinolytic therapy is indicated for patients with a diagnosis within 12 hours of presentation in the non-

operative settings, it is a poor reperfusion choice after non cardiac surgery due to the high risk of

postoperative bleeding. In the setting of perioperative STEMI, percutaneous intervention would be the

treatment of choice due to its lower risk for major hemorrhage. Patients with PMI most likely to benefit

include from percutaneous intervention or coronary bypass surgery are those with acute thrombotic

coronary occlusion reflected by sudden onset of symptoms and ST segment elevation on ECG. In most

situations PCI involves placement of a stent. However, even PCI involves use of anticoagulation which is

mandatory in this mode of treatment. It involves use of heparin, clopidogrel, aspirin, BBs and analgesics.

In NSTEMI, coronary intervention is not generally recommended unless the patient is at high risk or

hemodynamically unstable. Supportive therapy including use of BBs, aspirin, clopidogrel, statins and

hemodynamic support are generally used unless patient is in cardiogenic shock and coronary intervention

is mandated.

Summary

1. PMI is most common seen in the immediate postoperative period and is precipitated by

sympathetic surge commonly seen during this period.

2. ST segment depression type myocardial ischemia is most commonly seen after non cardiac

surgery although a significant number of patients with classical plaque rupture may also be seen.

3. Diagnosis of PMI is very vague and difficult. Elevation in cardiac biomarkers with or without ST

changes should portend postoperative cardiac complications.

4. BBs may be protective in prevention of PMI. However, unmonitored perioperative use of BB

may be harmful

27 | P a g e

5. Intravenous nitroglycerine in the perioperative and postoperative period is useful in prevention

and during treatment for myocardial ischemia.

6. IABP and coronary intervention should be sought primarily in patients with ST elevation type

ischemia whereas ST depression type ischemia should be managed conservatively.

References:

1. Landsberg G. The pathophysiology of perioperative myocardial infarction: Facts and

perspectives. J Cardiothorac Vasc Anesth 2003; 17: 90-100.

2. Badner NH, Knill RL, Brown JE et al. Myocardial infarction after noncardiac surgery.

Anesthesiology 199888:572-578.

3. Landsberg G, Beattie WS, Mosseri M et al. Perioperative myocardial infarction. Circulation

2009; 119: 2936-2944.

4. Little WC, Constantinescu M, Applegate RJ et al. Can coronary angiography predict the site of

subsequent myocardial infarction in patients with mild-to-moderate coronary artery disease?

Circulation 1988; 78: 1157-1166.

5. Biccard BM, Roseth RN. The pathophysiology of peri-operative myocardial infarction.

Anaesthesia 2010; 65: 733-741.

6. Landsberg G. Monitoring for myocardial ischemia. Bets Pract Res Clin Anaesthesiol 2005, 19:

77-95.

7. Browner WS, Li J, Mangano DT. In hospital and long term mortality in male veterans following

noncardiac surgery: the Study Perioperative Ischemia Research Group. JAMA 1992; 268: 228-

232.

8. Adams Jicard GA, Allen BT et al. Diagnosis of perioperative myocardial infarction with

measurement of cardiac troponin I. N Eng J Med 1994; 330: 670-674.

9. Thygesen K, Alpert JS, White SD et al. Universal definition of myocardial infarction. Circulation

2007; 116: 2634-2653.

10. Kim LJ, Martinez EA, Faraday N et al. cardiac troponin I predicts short term mortality in vascular

surgery patients. Circulation 2002; 106: 2366-2371.

11. Mangano DT, Layug EL, Wallace A et al. Effect of atenolol on mortality and cardiovascular

morbidity after non-cardiac surgery: Multicenter Study of Perioperative Ischemia Research

Group. N Eng J Med 1996; 335: 1713-1720.

12. Poldermans D, Boersma E, Bax JJ et al. The effect of bisoprolol on perioperative mortality and

myocardial infarction in high risk patients undergoing vascular surgery. N Eng J Med 1999; 341:

1789-1794.

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13. Priebe HJ. Perioperative myocardial infarction aetiology and prevention. Br J Anaesthsiol 2005;

95: 3-19.

14. POISE study group. Effects of extended release metoprolol succinate in patients undergoing non-

cardiac surgery (POISE trial): a randomized controlled trial. Lancet 2008; 371: 1839-1847.

15. 2009 ACCF/ AHA focused update on perioperative beta blockade: A report of the American

College of Cardiology Foundation / American Heart Association task Force on Practice

Guidelines. Circulation 2009 120: 2123-2151.

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Pathophysiology of respiratory failure

Dr. Nagamani Nambiar.V.V.

Consultant

Anaesthesiologist & Critical Care Physician

Kormbayil Hospital and Diagnostic Centre(P)Ltd.Kerala

Respiratory Failure

Definition: It is a syndrome in which Respiratory system fails in one or both of its gas

exchange function namely

Oxygenation and Ventilation.

The term respiratory failure implies the inability to maintain either the normal delivery of

oxygen to tissues or the normal removal of carbon dioxide from the tissues. There are actually

three processes involved: the transfer of oxygen across the alveolus, the transport of tissues (by

cardiac output), and the removal of carbon dioxide from the blood into the alveolus with

subsequent exhalation into the environment. Failure of any step in this process can lead to

respiratory failure

Types of Respiratory failure

1. Type 1 Respiratory failure

In this type of respiratory failure arterial oxygen tension is below 60 mm of Hg (Hypoxemic,

Pao2 < 60mm of Hg),PaCO2 may normal or low. This is the most common form of respiratory

failure, and it can be associated with virtually all acute diseases of the lung, which generally

involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failure are

cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage and

pulmonary fibrosis.Hypoxemia may be refractory to Oxygen therapy.

2. Type 2 Respiratory failure.

Hypercapnic respiratory failure (type II) is characterized by a PaCO2 higher than 50 mm

Hg. Hypoxemia is common in patients with hypercapnic respiratory failure who are

breathing room air. The pH depends on the level of bicarbonate, which, in turn, is

dependent on the duration of hypercapnia. Common etiologies include drug overdose,

neuromuscular disease, chest wall abnormalities, and severe airway disorders (eg, asthma

and chronic obstructive pulmonary disease ).

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3. Type 3 Respiratory failure

Type 3 respiratory failure can be considered as a subtype of type 1 failure. However, acute

respiratory failure is common in the post-operative period with atelectasis being the most

frequent cause. Thus measures to reverse atelectasis are paramount.In general residual

anesthesia effects, post-operative pain, and abnormal abdominal mechanics contribute to

decreasing FRC and progressive collapse of dependant lung units.

It can present as combined Oxygenation and Ventilation failure(PaO2 low and PCO2 high).

Alveolar Arterial Oxygen partial pressure is increased.(PAO2-PaO2)

Causes of post-operative atelectasis include:

decreased FRC

Supine/ obese/ ascites

anesthesia

upper abdominal incision

airway secretions

Therapy is directed at reversing the atelectasis are

Turn patient q1-2h

Chest physiotherapy

Incentive spirometry

Treat incisional pain (may include epidural anesthesia or patient controlled analgesia)

Ventilate at 45 degrees upright

Drain ascites

Re-expansion of lobar collapse

Avoid overhydration

Type 4 Respiratory failure

It due to cardiovascular abnormalities. Hypotension seen in septic shock patients leads to

hypoperfusion at the level of alveolus and respiratory muscles.

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DEPENDING ON THE TIME OF ONSET OF RESPIRATORY FAILURE IT IS

ALSO CLASSIFIED AS FOLLOWS:

ACUTE RESPIRATORY FAILURE

It is a sudden onset of respiratory failure.Usually associated with acute respiratory illness like

pneumonia,ARDS or sudden alveolar fluid filling as in acute left ventricular failure.Arterial

blood gas analysis shows PH usually less than 7.3,Hypoxemia,PaCO2 and bicarbonate which

is normal or low in initial stage.

CHRONIC RESPIRATORY FAILURE.

It is normally seen in patients who have pre existing respiratory disorders like COPD.Chronic

respiratory acidosis stimulates kidneys to reabsorb bicarbonate for compensation and keeps

the PH near normal. Renal compensation.ABG will show Hypoxemia,Hypercapnia,Increased

bicarbonate and PH usually above 7.35.

Other features like Polycythemia,Corpulmonale may be seen in patients with chronic

respiratory failure.

ACUTE ON CHRONIC RESPIRATORY FAILURE

Seen in advanced COPD patients.In an established chronic respiratory failure an acute

exacerbation of COPD results in this type of respiratory failure.ABG may show

hypoxemia,Hypercapnea,increased bicarbonate and PH usually < 7.3.

Pathophysiology of Respiratory failure.

Any of the following factors may be involved in the pathogenesis of the respiratory failure

Airway diseases

Alveolocapillary units

CNS,Brain stem

Peripheral Nervous System

Respiratory muscles

Chest wall and Pleura

Shock

Cardiogenic , Hypovolemic , Septic.

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Type 1 Respiratory Failure-Pathophysiology

Low inspired partial pressure of O2-This can occur in industrial settings in closed

spaces.If the inspired air has low Oxygen concentration than normal it can result in

hypoxemia.

Low barometric pressure- Seen in high altitude. Eg:At the summit of mount everest

Barometric pressure is only 256 mm of Hg hence berathing atmospheric air,one will have

PiO2 of 43 mm Hg and PaO2 28mm Hg. So it is not possible to stay alive here without

supplemental Oxygen.

Alveolar hypoventilation

Diffusion impairment

V/Q mismatch

Right to Left shunt

Causes of Type 1 Respiratory failure

Acute Asthma

ARDS

Pneumonia

Pulmonary embolism

Pulmonary Fibrosis

Pulmonary oedema

COPD

Impairment of diffusion: This means that equilibration does not occur between the PO2

in the pulmonary capillary blood and alveolar gas. Recall that the diffusion capacity of

the lung for a gas is equal to:

DL(gas) = net rate of transfer/Pgas betw. alveolus & capillary

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Under typical resting conditions, the capillary PO2 reaches that of alveolar gas when the red cell

is about one-third of the way along the capillary. Even when the capillary transit time is

shortened by exercise, the capillary blood equilibriates completely with alveolar air. However, in

some abnormal circumstances when the diffusion properties of the lung are impaired, the blood

does not reach the alveolar value by the end of the capillary. Diffusion limitation seldom causes

systemic hypoxemia at rest, but may cause hypoxemia during exercise when there is less time for

equilibration with alveolar gas.

Diseases in which diffusion impairment may contribute to hypoxemia include asbestosis,

sarcoidosis and diffuse interstitial fibrosis. Impaired diffusion is also likely to develop when PAO2

is abnormally low, such as at high altitudes. Here, the impairment occurs because the gradient for

O2-diffusion is low.

Carbon dioxide elimination is generally thought to be unaffected by diffusion abnormalities. This

is because the diffusion of CO2 is 20X faster than O2. Clinically, significant hypercapnia

(elevations in arterial PCO2) is never caused by a diffusion defect.

Hypoxemia can be easily corrected by breathing an enriched oxygen mixture.

V/Q ratio

V/Q ratio is amount of ventilation in relation to perfusion in any given part of the

lung.V/Q relates to the efficiency of lung units with which it resaturates venous blood

with O2 and eliminate CO2.

Since alveolar ventilation (VA) is normally 4 L/minute and Pulmonary capillary

perfusion(Q)is 5 L/minute,the over all V/Q ratio is 0.8.

V/Q for each alveolar-capillary unit can range from zero(no ventilation) to infinity

(no perfusion).Areas with no ventilation (V/Q=0) is referred as Intra pulmonary

shunt and areas with no perfusion is referred as alveolar dead space.

V/Q normally ranges between 0.3 and 3.3 with majority of lung areas close to 1.0.

Perfusion increases at a greater rate from nondependent to dependent part of the

lung when compared to ventilation.

V/Q at the top(Apex) of the lung 3.3 (Dead space)

Ventilation is more in relation to perfusion High V/Q areas (PAO2 132,PCO2 28 mm

of Hg)

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V/Q at the bottom(Base) of lung 0.3 (shunt)

Perfusion is more in relation to Ventilation Low V/Q areas (PAO2 89,PCO2 42 mm of

Hg)

When lung is inadequately ventilated and optimally perfused V/Q1

High V/Q Acts as alveolar dead space (Wasted Ventilation)

Normally dont affect gas exchange unless severe.

Ventilation Perfusion (V/Q) mismatch V/Q mismatch is the presence of a degree of shunt and a degree of dead space in the same

lung. It is a component of most causes of respiratory failure and is the commonest cause

of hypoxaemia.

Because of the complicated structure of the lungs, it is impossible to describe this

condition in anatomical terms. A patient with this condition is likely to have areas in the

lungs that are better perfused than ventilated and areas that are better ventilated than

perfused. This occurs in normal lungs to some extent. The difference in V/Q mismatch is

that the extent to which this occurs is significantly increased.

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OXYGEN DISSOCIATION CURVE

Because of the flat upper portion of the Oxyhaemoglobin dissociation curve , blood

leaving the relatively healthy alveoli will have an oxygen saturation of about 97%. Blood

leaving alveoli that do not have optimum V/Q ratios will have a much lower oxygen

saturations . The admixture of all the blood leaving the alveoli results low oxygen

saturations and hypoxaemia.

In general, this cause of respiratory failure responds to oxygen therapy, although the response

varies depending on the precise nature and size of the V/Q mismatch

Intra pulmonary Shunt

Deoxygenated blood (Pulmonary artery-Mixed venous) bypasses the alveoli and mixes with

oxygenated blood that has flowed through the ventilated alveoli resulting in decrease in arterial

oxygen content in the Pulmonary vein.

Types of Intrapulmonary shunt

True Shunt- V/Q = 0

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Total absence of gas exchange between Capillary blood and Alveolar gas.This can occur in intra

pulmonary arteriovenous fistulas.This does not respond to 100% oxygen.This shunt is equivalent

to the anatomic shunt between right and left side of the heart.

Venous admixture

Capillary flow does not equilibrate completely with Alveolar gas. Excessive perfusion in relation

to ventilation. Blood passes through low V/Q areas (V/Q

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Influence of shunt on Oxygen and Carbon dioxide tension

PaO2 falls progressively as the shunt fraction increases but PaCO2 remains constant until the

shunt fraction exceeds 50%.PaCO2 is often low in intrapulmonary shunting due to

hyperventilation triggered by disease process like sepsis or by accompanying hypoxemia.

In10 to 50% of shunt, increasing FiO2 has very minimal effect on PaO2.More than50% shunt

PaO2 is independent of changes in FiO2. Hypercapnia is seen when the shunt is >50% of

Cardiac output. A-a Oxygen partial pressure gradient increases in shunt.

Implication:

In ARDS with a very high shunt fraction, FiO2 can be kept to a minimum safe level without

further compromising arterial oxygenation thereby preventing pulmonary oxygen toxicity.

PaO2/FiO2 Ratio

It is used as an indirect estimate of shunt fraction.

PaO2/FiO2 < 200 = shunt fraction indication Qs/Qt >20% ,usually seen in ARDS.

PaO2/FiO2 >200 = shunt fraction indication Qs/Qt < 20%, Usually seen in Acute Lung

Injury.

Shunt and V/Q mismatch can be differentiated by administering 100% Oxygen or by

calculating the shunt fraction.

Shunt poorly responds to 100% Oxygen.

A-a gradient is high in shunt.

Alveolar to Arterial oxygen gradient= PAO2-PaO2

A-a PO2= (FiO2 X (PB-PH2O) - (PaCO2/R) ) - PaO2